Physiological and pharmacological inductors of HSP70 enhance the antioxidative defense mechanisms of the liver and pancreas in diabetic rats.

Heat preconditioning (HP) is a powerful adaptive and protective phenomenon and the heat stress proteins (HSPs) it produces are an important determinant for the development of diabetic complications. Aspirin has been reported to modulate heat shock response in different organisms through increased induction of HSPs and is also known to exert antioxidative and radical scavenging effects in diabetes. We estimated the effect of physiological (heat stress: 45 min at 41 ± 0.5 °C) and pharmacological (aspirin treatment) induction of HSP70 on several parameters of oxidative state in the pancreas and liver of diabetic rats. Diabetes increased HSP70 level and decreased poly(ADP) ribose polymerase (PARP), glutathione (GSH), and glutathione peroxidase (GPx) activities in the pancreas. In the liver, there was reduction of HSP70 level, GSH concentration, and CAT activity, while GPx and GR activity were enhanced. HP of diabetic rats caused an additional increase of HSP70, GSH, and antioxidant enzymes in both organs. Pre-treatment of HP-diabetic animals with aspirin led to an additional increase of PARP and HSP70. Both HP and aspirin, as physiological and pharmacological inductors of HSP70, respectively, enhanced the antioxidative defense mechanisms of the liver and pancreas in diabetic rats.